Tissue Expression Of The 6-Pyruvoyi Tetrahydropterin Synthase Gene In Adult Zebrafish,Danio Rerio.

Teleost is one of the poikilotherms that can display different kind of colours on their body. This is due to the presence of different types of chromatophores, a group of pigment containing cells that is distributed in the epidermal layer of skin and scales

A new class of pluripotent stem cell cytotoxic small molecules

10.1371/journal.pone.0085039PLoS ONE93-POLN

THE REGULATORY ELEMENTS OF HPV-16

Ph.DDOCTOR OF PHILOSOPH

Aminoglutethimide augments follicle-stimulating hormone-induced aromatase activity in cultured porcine granulosa cells

Endocrinology12252290-2298ENDO

Re-entering the pluripotent state from blood lineage: promises and pitfalls of blood reprogramming

Contains fulltext : 214027.pdf (publisher's version ) (Closed access)Blood reprogramming, in which induced pluripotent stem cells (iPSCs) are derived from haematopoietic lineages, has rapidly advanced over the past decade. Since the first report using human blood, haematopoietic cell types from various sources, such as the peripheral bone marrow and cord blood, have been successfully reprogrammed. The volume of blood required has also decreased, from around tens of millilitres to a single finger-prick drop. Besides, while early studies were limited to reprogramming methods relying on viral integration, nonintegrating reprogramming systems for blood lineages have been subsequently established. Together, these improvements have made feasible the future clinical applications of blood-derived iPSCs. Here, we review the progress in blood reprogramming from various perspectives, including the starting materials and subsequent reprogramming strategies. We also discuss the downstream applications of blood-derived iPSCs, highlighting their clinical value in terms of disease modelling and therapeutic development

Insights to Heart Development and Cardiac Disease Models Using Pluripotent Stem Cell Derived 3D Organoids

10.3389/fcell.2021.788955Frontiers in Cell and Developmental Biology978895

In Vivo Genome Editing as a Therapeutic Approach

Genome editing has been well established as a genome engineering tool that enables researchers to establish causal linkages between genetic mutation and biological phenotypes, providing further understanding of the genetic manifestation of many debilitating diseases. More recently, the paradigm of genome editing technologies has evolved to include the correction of mutations that cause diseases via the use of nucleases such as zinc-finger nucleases (ZFN), transcription activator-like effector nucleases (TALENs), and more recently, Cas9 nuclease. With the aim of reversing disease phenotypes, which arise from somatic gene mutations, current research focuses on the clinical translatability of correcting human genetic diseases in vivo, to provide long-term therapeutic benefits and potentially circumvent the limitations of in vivo cell replacement therapy. In this review, in addition to providing an overview of the various genome editing techniques available, we have also summarized several in vivo genome engineering strategies that have successfully demonstrated disease correction via in vivo genome editing. The various benefits and challenges faced in applying in vivo genome editing in humans will also be discussed

Prox1 Is a Novel Coregulator of Ff1b and Is Involved in the Embryonic Development of the Zebra Fish Interrenal Primordium

Steroidogenic factor 1 (SF-1) plays an essential role in adrenal development, although the exact molecular mechanisms are unclear. Our previous work established that Ff1b is the zebra fish homologue of SF-1 and that its disruption by antisense morpholinos leads to a complete ablation of the interrenal organ. In this study, results of biochemical analyses suggest that Ff1b and other Ff1 members interact with Prox1, a homeodomain protein. Fine mapping using site-directed mutants showed that this interaction requires an intact Ff1b heptad 9 and AF2, as well as Prox1 NR Box I. In vivo, this physical interaction led to the inhibition of Ff1-mediated transactivation of pLuc3XFRE, indicating that Prox1 acts to repress the transcriptional activity of Ff1b. In situ hybridization demonstrates that prox1 colocalizes with ff1a and ff1b in the liver and interrenal primordia, respectively. Embryos microinjected with prox1 morpholino displayed a consistent partial reduction of 3β-Hsd activity in the interrenal organ, while ff1b morpholino led to a disappearance of prox1. Based on these results, we propose that during the course of interrenal organogenesis, Prox1 functions as a tissue-specific coregulator of Ff1b and that the subsequent inhibition of Ff1b activity, after its initial roles in the specification of interrenal primordium, is critical for the maturation of the interrenal organ